Objective To explore the mechanism of lipid metabolism disorder promoting the progress of lung cancer based on the oxidized low density lipoprotein(ox-LDL)/human lectin-like oxidized low density lipopro-tein receptor 1(LOX-1)signaling pathway.Methods Eighty-one identified lung adenocarcinoma tissues with paired adjacent non-cancerous tissues(at least 5 cm away from the tumor)were collected from our hospital,and the expression of LOX-1 was detected by immunohistochemistry.LOX-1 was overexpressed in lung adenocarcinoma cell lines(A549 and H1299 cells).Cell invasion ability was measured by Transwell.Cells were treated with different concentrations of oxLDL,and cellular LOX-1 expression was investigated.Results LOX-1 staining in the tumor was significantly stronger than that in the non-cancerous tissue samples(99.4 vs.16.2 for median H score,P<0.001).High LOX-1 expression was significantly correlated with low survival(P<0.001).As compared with the patients without lymph node metastasis,those with lymph node metastasis had higher LOX-1 level(83.2 vs.121.1 for median H score,P<0.01).Overexpression of LOX-1 in lung cancer cells significantly promoted the number of invasive and metastatic cells(P<0.01).In addition,LOX-1 was an essential functional target for oxLDL-induced metastasis of lung cancer cells.Itatinib inhibited the metastasis of LOX-1 overexpressed A549 in vitro.Conclusions With an increase in oxLDL level,the expression of LOX-1 increases.Up-regulation of LOX-1 promotes metastasis of lung cancer,and its mechanism may be related to activation of the JAK1/STAT6 signaling pathway.

Objective To investigate the influence of the Janus kinase-signal transducer and transcription activator(JAK-STAT)signaling pathway mediated by Kruppel-like factor 14(KLF14)on the prognosis of non-small cell lung cancer(NSCLC).Methods From January 2018 to September 2019,NSCLC tissues from 80 patients and malignancy-free paracancerous tissues from 25 patients were collected.Medical follow-up ended in April 2023.Immunohistochemistry was used to detect the expression of KLF14 in tissues,and the patients were divided into a high-expression group and a low-expression group according to the median level of KLF14 expression.Over-expres-sion or knock-down of KLF14 and JAK1 was achieved by transfection of KLF14 and JAK1 overexpression plasmid in A549 cells and transfection of KLF14 and JAK1 specific short hairpin RNA(shKLF14 and shJAK1)in HCC827 cells.The proliferation activity of cells was analyzed by cell clone formation test.Transwell analyzed the migration and invasion of cells.Results As compared with the normal paracancerous tissues,the expression of KLF14 in NSCLC tissue decreased(P<0.001).The low expression of KLF14 was significantly correlated with tumor diameter of>3 cm,lymph node metastasis and clinical stage Ⅲ(P<0.05).There was a significant difference in the overall survival rate between the high KLF14 expression group and the low KLF14 expression group,and the patients with low KLF14 expression had poor prognosis(P = 0.039).After overexpression of KLF14,the proliferation ability of A549 cells and the number of migration and invasion of these cells decreased significantly(P<0.05);while after knock-down of KLF14,the proliferation ability of HCC827 cells and the number of migration,and invasion of these cells increased significantly(P<0.05).As compared with Vector + KLF14 group,the number of colonies,migration and invasion of A549 cells in JAK1 + KLF14 group increased significantly(P<0.05).As compared with shNC + shKLF14 group,the number of colonies,migration and invasion of HCC827 cells in shJAK1 + shKLF14 group decreased significantly(P<0.05).Conclusions Low expression of KLF14 is associated with poor overall survival in NSCLC patients.Up-regulation of KLF14 significantly inhibits the proliferation and metastasis of lung cancer cells in vitro,and its mechanism may be related to inhibition of the JAK-STAT signaling pathway.

Angiokinases, such as vascular endothelial-, fibroblast- and platelet-derived growth factor receptors (VEGFRs, FGFRs and PDGFRs) play crucial roles in tumor angiogenesis. Anti-angiogenesis therapy using multi-angiokinase inhibitor has achieved great success in recent years. In this study, we presented the design, synthesis, target identification, molecular mechanism, pharmacodynamics (PD) and pharmacokinetics (PK) research of a novel triple-angiokinase inhibitor WXFL-152. WXFL-152, identified from a series of 4-oxyquinoline derivatives based on a structure-activity relationship study, inhibited the proliferation of vascular endothelial cells (ECs) and pericytes by blocking the angiokinase signals VEGF/VEGFR2, FGF/FGFRs and PDGF/PDGFR simultaneously . Significant anticancer effects of WXFL-152 were confirmed in multiple preclinical tumor xenograft models, including a patient-derived tumor xenograft (PDX) model. Pharmacokinetic studies of WXFL-152 demonstrated high favourable bioavailability with single-dose and continuous multi-dose by oral administration in rats and beagles. In conclusion, WXFL-152, which is currently in phase Ib clinical trials, is a novel and effective triple-angiokinase inhibitor with clear PD and PK in tumor therapy.

Purpose: Microtubule-associated protein 1 light chain 3B (LC3B) serves as a key component of autophagy,which is associated with the progression of carcinoma. Yet, it is still unclear whetherLC3B is also an independent risk factor for intrahepatic cholangiocarcinoma (ICC). We aimto explore the predictive value of LC3B on prognosis of ICC, and to establish a novel andavailable nomogram to predict relapse-free survival (RFS) and overall survival (OS) for thesepatients after curative-intent hepatectomy. Materials and Methods: From August 2004 to March 2017, 105 ICC patients were eligibly enrolled in the ThirdAffiliated Hospital of Sun Yat-sen University. Preoperative clinical information of enrolledpatients was collected. Expression LC3B in the ICC specimen was detected by immunohistochemistry. Results: The 5-year RFS and OS in this cohort were 15.7% and 29.6%, respectively. On multivariateCox regression analysis, independent risk factors for 5-year OS were cancer antigen 125,microvascular invasion, LC3B expression and lymph node metastasis. Except for the above4 factors, neutrophil/lymphocyte ratio and tumor differentiation were independent factorsfor 5-year RFS. The area under the curve of nomograms for OS and RFS were 0.820 and0.747, respectively. Conclusion The nomograms based on LC3B can be considered as effective models to predict postoperativesurvival for ICC patients.

Objective: To develop a health management system for outpatient follow-up of kidney transplant patients. Methods: Access 2010 database sotfware was used to establish the health management system for kidney transplantation patients in Windows XP operating system. Database management and post-operation follow-up of the kidney transplantation patients were realized through 6 function modules including data input, data query, data printing, questionnaire survey, data export, and follow-up management. Results: The system worked stably and reliably, and the data input was easy and fast. The query, the counting and printing were convenient. Conclusion: Health management system for patients after kidney transplantation not only reduces the work pressure of the follow-up staff, but also improves the effciency of outpatient follow-up.

Host genetic, environmental and viral factors are classified as three categories that determine clinical outcomes of hepatitis B virus (HBV) infection. The objective of this study was to detect the associations between polymorphisms rs346473 and rs346482 in Rho GTPase-activating protein 24 (ARHGAP24) gene and disease progression of HBV infection in Han Chinese population. These two SNPs were found by our DNA pooling using Affymetrix Genome-Wide Human Mapping SNP6.0 Array in HBV carriers, and verified by using TaqMan 7900HT Sequence Detection System with 758 progressed HBV carriers versus 300 asymptomatic HBV carriers (AsC) in a discovery phase and 971 progressed HBV carriers versus 328 AsC in a replication phase. Multivariable logistic regression revealed that individuals with genotype TT at variant rs346473 displayed remarkable correlations with disease progression of HBV infection both in the discovery phase (OR, 2.693; 95% CI, 1.928-3.760; P=6.2×10(-9); additive model) and the replication phase (OR, 1.490; 95% CI, 1.104-2.012; P=9.0×10(-3); additive model). These two SNPs were in strong linkage disequilibrium with D'=0.99 and r (2)=0.951, and haplotype TT disclosed an increased susceptibility to HBV progression (OR, 1.980; 95% CI, 1.538-2.545; P=8.1×10(-8)). These findings suggest that polymorphism rs346473 in the ARHGAP24 gene might be a part of the genetic variants underlying the susceptibility of HBV carriers to disease progression.

Host genetic,environmental and viral factors are classified as three categories that determine clinical outcomes of hepatitis B virus (HBV) infection.The objective of this study was to detect the associations between polymorphisms rs346473 and rs346482 in Rho GTPase-activating protein 24 (ARHGAP24) gene and disease progression of HBV infection in Han Chinese population.These two SNPs were found by our DNA pooling using Affymetrix Genome-Wide Human Mapping SNP6.0 Array in HBV carriers,and verified by using TaqMan 7900HT Sequence Detection System with 758 progressed HBV carriers versus 300 asymptomatic HBV carriers (AsC) in a discovery phase and 971 progressed HBV carriers versus 328 AsC in a replication phase.Multivariable logistic regression revealed that individuals with genotype TT at variant rs346473 displayed remarkable correlations with disease progression of HBV infection both in the discovery phase (OR,2.693; 95％ CI,1.928-3.760; P=6.2× 10-9;additive model) and the replication phase (OR,1.490; 95％ CI,1.104-2.012; P=9.0× 10-3; additive model).These two SNPs were in strong linkage disequilibrium with D'=0.99 and r2=0.951,and haplotype TT disclosed an increased susceptibility to HBV progression (OR,1.980; 95％ CI,1.538-2.545;P=8.1× 10-8).These findings suggest that polymorphism rs346473 in the ARHGAP24 gene might be a part of the genetic variants underlying the susceptibility of HBV carriers to disease progression.

Objective To explore the expression of KAI1/CD82,E-cadherin and β-catenin in endometrial carcinoma,and to investigate their correlations to clinicopathological parameters of endometrial carcinoma. Methods The expressions of KAI1/CD82,E-cadherin and β-catenin in 76 specimens of endometrial carcinoma,15 specimens of atypical endometrial hyperplasia and 20 specimens of proliferative endometrium were examined by immunohistochemical envision technique.Their correlations to clinicopathological parameters of endometrial carcinoma were statistically analyzed. Results Compare to normal proliferative phase endometrium and atypical endometrial hyperplasia,the expression of KAI1/CD82 in endometrial carcinoma was significantly decreased(P ＜0.01),the abnormal expression of E-cadherin and β-catenin in endometrial carcinoma were significantly higher(all P <0.01).In endometrial carcinoma,the expression of KAI1/CD82 was negative correlated with histological grade and depth of myometrial invasion(P <0.01,P <0.05); The abnormal expression of the E-cadherin is related to histological grade and type(P <0.01,P<0.05); The abnormal expression of β-catenin was positively correlated with histological grade and FIGO stage(P ＜0.01 ,P <0.05).The down-regulation expression of KAI1/CD82 was closely associated with the abnormal expression of E-cadherin and beta-catenin in endometrial carcinoma(P <0.01,P <0.05). Conclusion The down-regulation of KAI1/CD82 and the aberrant expression of E-cadherin and β-catenin could be involved in the development of endometrial carcinoma.The loss or reduced expression of KAI1/CD82 was closely associated with the abnormal expression of E-cadherin and β-catenin in endometrial carcinoma.

How to detect the P300 component in EEG accurately and instantly is a hot problem in the research field of Brain-Computer Interface. In this paper, an algorithm based on F-score feature selection and support vector machines was introduced for P300 detection. Using F-score feature selection method, we reduced input features to overcome the shortcoming of support vector machines in terms of low detection speed, and then implemented the detection of P300 component with support vector machines, which have good classification performance. The algorithm was tested with a P300 dataset from the BCI competition 2003. The results showed that the algorithm achieved an accuracy of 100% in P300 detection within five repetitions, and the detection speed of this algorithm was 2 times higher than that of the traditional support vector machines algorithm without F-score feature selection.
Algorithms ; Electroencephalography ; methods ; Event-Related Potentials, P300 ; physiology ; Humans ; Pattern Recognition, Automated ; methods ; Principal Component Analysis ; Signal Processing, Computer-Assisted

Aim To observe the fluctuation of uric acid in serum after replicating rat hyperuricemia model with hypoxanthine, uricase inhibitor singly or combined. Discuss the method of acute hyperuricemia replication on rats. Method Hypoxanthine was administered via stomach, uricase inhibitor was injected intraperitoneally, then inspect the uric acid in serum at different periods of time. Results When we combined hypoxanthine with uricase inhibitor, the uric acid in serum of different dose groups was higher than control group after 3 hours(P